On Gout as a Peripheral Neurosis

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ON GOUT

ON GOUT

AS A PERIPHERAL NEUROSIS

J J J

J - J

^ O J ^ J

J J 3 -'

^ J V -< J J -*

BY

WILLOUGHBY FRANCIS WADE

Fellow of the Royal Colleor of Physicians of London, &c.,
Consulting Physician to thr.Grnkkal Hospital,

Birmingham.

SiMPKiN, Marshall, Hamilton, Kbnt and Co., Limitbd.

BIRMINGHAM :
Cornish Brothers, New Street.

1893.

J

J

CHAPTER L

TT is desirable to state the scope and object
-^ of this essay. To do this clearly and
briefly it is necessary to glance at the theories
which have been or are current in regard to
gout, of these there are broadly three. Firstly
that which refers it to impurity of the blood, or,
to maintain an old word which corresponds so
little to modern conceptions as to have become
almost obsolete, the humoral theory. Secondly
the neural or nerve theory, which views gout
as depending upon a disordered condition of the
nervous system. Thirdly the neuro humeral
theory, which combines the two first and regards
gout as being due partly to disorder of the
blood and partly to. disorder of the nervous
system.

Much as we know about gout, it would be
idle to deny that there are still wide gaps or

B

J

2 CHAPTER I.

lacuna in our knowledge, many questions which
we cannot at present answer. It is impossible
to foresee what answer science will give, when
she is able to give any, to these questions. It
is therefore impossible to foresee in what way or
to what extent these answers, when they come,
will necessitate a new theory, or a modification
of any one that we at present form.

From the standpoint of our present knowledge
it seems to me impossible to be satisfied with
any theory less comprehensive than the neuro-
humeral one.

It may here be justly remarked that " the
J system " is too vague a term, for this
consists of collections of grey matter in
,in, in the medulla, in the cord and in
>\ia ganglia ; of white matter which is in
ate apposition with the various grey foci,
white matter which extends to the more
parts of the body as nerve trunks, and
ninute endings of these in the tissues.
y," an objector may say " you ought if
: me to accept your nerve-theory to tell

CHAPTER I. 3

me in which one of these various parts you
locate the disease and for what reasons you fix
on that particular part." The nearest approach
to an answer which has heen given "to this
fair objection is that it is " some nerve centre."
Now I am not prepared to deny that this may
be so. On the contrary, it would seem to me
to be flying in the face of some of the most
certainly ascertained clinical facts to deny that
the highest centres may be concerned in the
production of gout in particular instances.
Because few facts in connection with gout are
more certain than that excessive brain work,
and care and anxiety are in some instances the
apparent producers of the gouty attack, though
whether by augmenting the gouty poison in the
blood or by some direct action on the part which
is attacked is by no means so certain. There are
truly no lower centre or centres of which^ with
certainty, as much can be said. But it would be
fatuous to contend that evidence exists to show
that the higher centres are in all cases the seat
of origin of gout whether directly or indirectly.

4 CHAPTER I.

At all events I certainly do not do so. So that
we are confronted with two facts. One that
there are a multiplicity of phenomena which
indicate that the nervous system is implicated
in gout. The other, that we seek in vain for
any precise indication that any one portion of
the central nervous system can be identified as
being, whether directly or indirectly, that which
is so implicated, except in an occasional way.
It was the pressure of this dilemma that
caused me to turn my attention in another
direction.

A frequently occurring, and a most obvious
feature of gout is its invasion of the joints,
and the great numerical preponderance of
instances in which the great toe is attacked as
compared with any other joint. Any theory of
gout which does not explain this superior
frequency must be stamped with inadequacy.
On the other hand any one which does, at once
establishes a claim to attentive consideration.

An investigation of the anatomy of the joint
only served to corroborate Ebstein's dictum^

CHAPTER I.

that there is no difference between it and any
other joint in the body. That is to say no
minute nor any coarse structural differenc«
which throws light upon its pathological reaction
to the poison of gout. But on the other hand
I was struck by certain features of its environ-
ment, which we have all known since we were
students, but to which we have never given
heed. Looked at from the point of view in
which I then stood they assumed a possible
importance. They recalled to my mind an
isolated clinical observation of previous years
and they determined me to institute a more
searching and minute examination of living
cases of the disease. It Is the result of such
investigations and the inferences to be drawn
from them that are related in sub;sec

CHAPTER 11.

"%VTE are familiax with the swelling, redness
* ^ and extreme sensitiveness of the skin
over the toe-joint in acute gout. We know
also that a similar condition is observed often
to exist in the neighbouring skin and soft parts.
As this condition subsides a time comes when
the patient will, though reluctantly, allow the
part to be cautiously handled. It is a good
many years since it became known to me, that
the tenderness did not like the redness and
swelKng abate equably over all the surface. In
some places the skin remained tender in others
not. The tenderness had a '* patchy" character.
There v>/as not always a corresponding difference
of appearance in the skin. This long remained
to me an isolated clinical fact, unexplained
though of pretty constant occurrence.

CHAPTER II. 7

Subsequently, as I have said, my attention
was again attracted to this subject and I
investigated it more closely, I then found that
the residual tenderness might not only be in
the shape of spots and patches, but also in that
ot lines. I will cite as examples of this latter
condition two cases which have been under my
care this year.

One was a lady, aged about sixty, for twelve
years subject to attacks of acute gout in the
great toes and other parts. Her heart, lungs
and stomach were failing and she died a few
days after my only visit. I found that wi''^'-
a few days she had had gout in the left
which had entirely recovered. Before it
well gout had come on in the right toe, w
was still swollen and painful. From the
of the toe for about one and a half inches t
extended a narrow line of acute tenden
There was no super-jacent redness or swel
Pressure on each side of this line was absoh
painless. The line itself was apparently e
in breadth to the diameter of an ordinary i
steel knitting pin.

8 CHAPTER 11.

The second case occurred before the one
above described.—

A gentleman, aged fifty-eight, had a first
attack of acute gout in the left gi'eat toe,
extending also a little above it. After a few
days' treatment this abated, and the great toe-
joint admitted of passive movement in all
directions, the opposing surfaces of the two
bones being at the same time firmly pressed
against each other. But a line of tenderness,
similar to that described in the former case,
remained. It started from the base of the great
toe and extended slantingly across the foot as
far as the centre of the bend of the ankle. The
tenderness disappeared at the rate of about
three-quarters of an inch a day from above
downwards. There was during this period no
diminution of the tenderness in the part which
remained tender. For the sake of clearness I
have described this case as it appeared after all
redness and swelling had disappeared. For the
sake of accuracy I must now state that the line
of tenderness existed while the redness and

CHAPTER TI. 9

swelling still remained over its distal part. The
upper portion lay in a part which had not been
red, swelled, or painful.

We have now to determine the anatomical
seat of this tenderness. If we refer to Swan's
*^ Demonstration of the nerves of the human
body," we find (plate xxiv, fig. 2,) a nerve
which he describes thus " No. 4 Inner division
of the dorsal branch of the peroneal nerve,
giving filaments to the foot, the inner side of
the great toe, the outer side of the second and
the inner side of the third toes." But if we
look again at Swan's plate we find that the
nerve No. 4 divides just at the middle of the
lower border of the anterior annular ligament
into two branches. Of these one runs
slantingly across the foot to the base of the
great toe and it is this branch which is
distributed to the great toe. The other branch
is distributed to the other toes.

According to this authority then, this nerve
follows a course which coincided with the line
of tenderness, the breadth of which, so far as we

10 CHAPTER II.

can judge, corresponded with that of the nerve.
The tendon of the long extensor of the great
toe runs a somewhat similar course but its
width is several times that of the nerve. So
much so that I cannot think that, if it were
tender, the tenderness could with any accuracy
be spoken of as a " narrow line." Voluntary
movements of the great toe in the second case
were quite painless, which is probably incon-
sistent with an acutely tender state of the
extensor tendon.

The veins over an acutely gouty joint no
doubt often appear to be tender. Whether this
tenderness is intrinsic or merelv results from
the distension affording greater resistance
behind the skin when this is struck, and so
enhancing the skin tenderness it is not needful
here to enquire. For there was no venous
distension present in either case at the time
spoken of

I submit then that there is good ground for
the conclusion that the nerve was the anatomical
seat of this tenderness.

CHAPTER II. 11

Two farther questions of great importance
now arise. Firstly what is the nature of this
neuropathy? Secondly what is its relation to
the gouty joint ? The consideration of theee
questions will be conveniently postponed till
after attention has been called to some other
clinical facts.

Gout as affecting the hands, may as regards
its acute, subacute, or chronic phases, be
divided into five classes. First — Gout in the
knuckles : Second — In the back of the hands :
Third — In the ball of the thumb : Fourth — In
the hypothenar region : Fifth — Those causes in
which two or more of the previous classes occur
at the same time.

My first observations in this clinical division
were made upon myself, for I have twice had
gout in the root of each thumb, and once in the
right hypothenar region. But only two of these
attacks have occurred since my attention has
been directed to these investigations, and I was
at the same time sufficiently well to investigate
my symptoms. In the hypothenar attack tha

12 CHAPTER II.

pain and tenderness in the part itself were,
though quite distinct, by no means severe.
But on examination I found that there was
extreme tenderness on pressing the wrist, just
to the radial side of the pisiform bone. The
pressure left an aching at the part where it was
applied, and produced for some hours an increase
of the pain and tenderness in the hypothenar
region. Pressure here, in healthy persons,
produces a contraction of the abductor muscle
of the little finger. This is not absent when in
gouty persons there is also tenderness on
pressure. From this, as well as from anatomical
considerations, it is to be inferred that it is the
ulnar nerve which is the seat of this tenderness.
Here is another instance : Meeting in the street
a gentleman, set. fifty-two, who has for some
years suffered a good deal from acute joint gout,
he told me that during the preceding night gout
** had come out" in his hand, indicating the
hypothenar region. I said give me your hand.
As I was slipping my thumb under his cufi* he
said " Oh no its not there, there is nothing

OnAPTER II. 13

there." By this time I had my thumb in
positioQ and gave a squeeze. He snatched his
hand away, exclaiming in a voice too loud for
the street '* Oh, by gad there is though ! " and
added " I never felt anything there till you
pressed it." I have mentioned this case in
somewhat trivial detail to show that there was
no collusion or self-deception.

A medical man set. seventy-two had for several
weeks remittent and chiefly nocturnal pain and
swelling in the knuckles, and paiufulness on
usage, of the right hand. He was much
surprised on finding that pressure at the point
indicated was extremely painful and that the
pain remained there for some hours^ after. He
was also an example of the next form of
tenderness, namely, that in connection with the
thumb. My first observation of this form was
made on myself There was a good deal of
pain all round the ball and root of the thumb,
with redness and some swelling, movement was
painful. Keeping the bones straight and
holding the first phalanx no pain was produced

7

14 CHAPTER II.

by pressing firmly and moving the joints, so far
as that could be done withuot disturbing the
soft parts- Pressure on the wrist in the interval
between the tendons of the two extensors of
the thumb was acutely painful, it also much
aggravated the painfulness of the thumb for
some hours after. It is to be noted with regard
to the case of the medical man at seventy-two
that just at the wrist-joint the ulnar nerve gives
off a deep branch which supplies inter alia the
joint between the metacarpal bone and the first
phalanx of the ring finger, of the second finger
and of the fore-finger (Swan, pi. xxii, fig, 2,
Nos. 28, &c.) I have also found tenderness in
the nerves which run one on each side near to
the dorsum of the fingers and one on each side
of their palmar aspects. If there should, as
there may, be general tenderness of the fingers,
the sites of these nerves cannot be distinoruished.
So far as I have been able to test it, and that
has been in about a dozen consecutive cases,
tenderness will almost certainly be tound in one
or more of the situations indicated when there

CHAPTER II. 1 5

is or recently has been gout in or flying about
the hand or fingers. There is also another
place where tenderness may be found. This is
about the centre of Ihe dorsum of the wrist,
just where Swan shows a branch of the ulnar
nerve, joining one from the radial.

Let us now turn to another division of the
subject. Persons who are in a gouty condition
are subject to pain and tenderness, recurring at
irregular intervals and of very variable, some-
times persistent, sometimes of only momentary
duration, about the ball of the great toe. This
tenderness is specially felt in walking. This
pain is, by common consent and repute, located
in the metatarso -phalangeal joint of that toe.

This view receives primd facie support from
physical examination. For undoubtedly pressure
applied over the upper aspect of the joint, or at
its side, or on the lower aspect of the joint may
elicit a complaint of tenderness in one or more of
these situations. I myself have for years been
from time to time subject to this affection. And
for years in dutiful submission to current

16 CHAPTER II.

teaching looked upon the joints as the seat of
the trouble. The circumstances previously
stated led me to investigate the matter impar-
tially and de novo. What did I find ? In the
first place that passive movement of the joint
surfaces upon themselves, the first phalanx held
firmly between finger and thumb and all
possible pressure made upon the joint was
absolutely painless. There was no evidence of
fluid in the joint. It is impossible without
cutting into it to obtain stronger evidence that
the joint was healthy.

On critical examination the tenderness was
and will be found as above mentioned in one or
more of three situations. If we look at Swan's
demonstrations (pi. xxiv., fig. 2), we find that
two branches of the internal plantar nerve lie
one to the outer side and one to the inner side
of the plantar aspect of the great toe. I have
demonstrated to myself on myself many scores
of times that what appears on ofF-hand examin-
ation to be tenderness in the great toe-joint is
really one or two lines of tenderness occupying

CHAPTER II. 17

the site of these two nerves. When there is
only one Hne it is commonly, but not invariably,
the inner one Between these two lines is to
be felt the bone absolutely indolent. No doubt
if we press over the joint we shall find tender-
ness, because the nerves run across the joint.
But we shall also commonly find an equal degree
of tenderness in both the distal and the
proximal sections of these nerves quite away
from the joint. With regard to the tenderness
over the superior aspect of the joint enough has
been said in speaking of it in acute gout. Only
adding that it occurs in the absence of that
disorder. The side tenderness I have found not
only under the circumstance with which we are
now dealing but also on the abatement of acute
gout. It is I think probably situated in branches
of the peroneal (so called by Swan and by
Quain and Ellis external-popliteal) nerve. Or it
may be in the saphenous nerve. Probably the
former, as it has not appeared to me to have
sufficient longitudinal extension to be situated
in the latter.

18 CHAPTER II.

There is another part in which I have found
tenderness. In most accounts of gout we find
mention of pain and tenderness in the sole of the
foot as occurring in certain cases. This tender-
ness is always described as being situated in the
plantar fascia. Nor would I deny that such
may be the case. But on the other hand I
have found a line of tenderness near the iuner
margin of the sole of the foot. On referring to
Swan (pi. XXV., fig. 3, No. 8), we find that just
in this situation lies a slender nerve which he
thus describes. " A branch of the branch five
of the inner plantar nerve, to terminate in the
joint of the great toe between the metatarsal
bone and the first phalanx." " Branch five " is
the nerve which has been referred to as running
on the inner side of the inferior aspect of the
great toe. It may be argued that if the in-
flammation of the great toe-joint depended upon
a morbid condition of this nerve, it should in all
cases be found to be tender. I shall deal with
this argument hereafter.

I have repeatedly verified in other persons
the fact that tenderness supposed to be in the

CHAPTER II. 19

toe-joint was really located in one of these
nerves and not in the joint.

Pains and tenderness in the thick of the
heel — I am not now alluding to the tendo
Achillis — are common in gouty persons. Few
old gouty patients are not familiar with their
occurrence from time to time, though they often
do not think enough of it to mention it to the
doctor. The outer half of the heel receives its
nervous supply from a nerve compounded of a
" communicating tibial branch of the sciatic
nerve " and a " cutaneous branch of the peroneal
nerve, receiving the communicating tibial"
(Swan, pi. XXV., fig. 2, Nos. 20 and 21). This
joint nerve in its course lies behind the outer
ankle.

The inner half of the heel is supplied by the
posterior tibial which lies behind the inner aokle.

Now I have often noticed in myself the
following facts, which however I have not yet
had an opportunity of verifying in other cases.
The pain commonly of an aching, sometimes of
a burning, character, a superficial and also a

20 CHAPTER II.

deep-seated tenderness, may occupy either one
lateral half of the heel or both halves at the
same time. In the latter case they may not be
of the same intensity on each side. Distinct
tenderness may be correspondingfly present
behind one or both ankles, presumably in the
nerve - trunks above mentioned. But such
tenderness is not invariably present.

Tenderness in all the above mentioned
situations, both in the feet and in the hands
and wrists may from time to time be found even
when the patient has not felt it during their
ordinary use. Its presence is of importance as,
in my opinion, identifying as gouty, visceral or
other symptons which we should otherwise only
with uncertainty suspect to be so.

These pains are notoriously fugitive, often a
mere momentary dart. The tenderness also is
often inconstant, present and absent in the
course perhaps of half an hour; or if not
absolutely vanishing yet varying much in
intensity. This I have repeatedly observed in
myself.

CHAPTER II. 21

I desire now to turn to another matter,
namely the connection of articular gout with
injury. This connection is well known, but I
am not sure that it habitually receives as
minute attention as it deserves. I shall briefly
catalogue the various circumstances under which
it presents itself.

We may divide these cases into three classes.
First — Gross mechanical injuries such as sprains,
bruises or blows. Second — Minor mechanical
injuries. Third — What may be described as
physiological injuries. Of the first class we
have several varieties. First — When a first
attack of gout appears in a part long after the
injury has occurred. A clergyman sprained his
right ankle badly in running down stairs. It
was not till fifteen years after that he, being
hereditarily gouty, had an attack of gout
(traceable to worry) and that was in this ankle.
Second — cases in which gout immediately or very
shortly follows the injury and is confined to the
injured part. This happened to a gouty surgeon
who not very severely sprained his right knee

22 CHAPTER II.

by being tbrown from his tricycle. In two or

three days the knee, in which there had

remained a little pain from the time of the

accident became the seat of an acute and very

long continued attack of gout. Third — Cases in

which gout appears in other joints as well as in

the injured one. A gentleman set. fifty who had

had, during the previous twelve years, several

severe attacks of gout, twisted his ankle, it

remained very painful and soon became swollen,

during the night the other ankle also became

swollen and painful, and he then recognised

that he had gout in both joints. This opinion

was confirmed by the Italian doctor whom he

called in, he being at the time at Turin. He

* was confined to bed for sis weeks. Another

gouty man of about the same age fell and

twisted his knee, it very shortly after was seized

gout This migrated to the other

squently to each ankle, and finally

I the knee first affected. He had a

troublesome attack, lasting many

lady set. eighty-four, who was of a

CHAPTER II. 23

gouty stock, but had never had gout, was
thrown from a high dog-cart. She did not know
exactly how she fell, but not on her back. In
two or three days she had very acute gout in
both wrists and subsequently in both elbows.

Fourth — Cases in which there is a long
interval between the accident and the gout, but
not entire freedom from symptoms due to the
accident. While getting into my carriage with
the right foot on the step the horses gave a
start. From that time with variations in
degree, but rarely if ever complete absence, my
knee was more or less but never severely painful
on movement. The pain was in a transverse
line just above the joint and there was also
tenderness. These symptoms lasted for ten
months. At the end of that time I went to
Buxton and put myself under the care of my
friend Dr. Robertson. The baths relieved
without entirely curing the knee and quite
relieved the general arterial tension which had
been all the time unduly high. Within a week
of my return home acute inflammation of the

24 CHAPTER II.

knee-joint, with great effiision, occurred. It is
worth mentioning that at Buxton in a bath at
98° the water appeared to the knee to be
several degrees colder than it did to any other
part of the body. When I have pain in
the heels hot baths, whether whole or partial,
generally feel hotter to the heel than to other
parts. This form of altered sensibility, which I
have known to occur in other persons points to
an abnormal state of the sensory nerves.

Fifth — I am not cognisant of any case in
which injury to one joint has appeared to cause
gout not in it but in another.

The second class comprises those cases in
which minor injuries appear to cause gout. It
is hardly necessary to point out that the
distinction between " gross " and " minor "
injuries is of a somewhat arbitrary character.
These cases present many varieties.

First — Production of gout by the use of
parts, as of the thumb from writing, or from
repeated use of it for lifting purposes. Of both
these I have had experience in my own person.

CHAPTER II. 25

Second — Aggravation of gout by use of the
part. A widow lady was much addicted to
crochet work. She used to have attacks of gout
in the right hand, which unless or until they
were so severe as to make it impossible she did
not allow to interrupt her work. For two years
her left arm and leg have been absolutely
paralysed. During that time she has often
been in a gouty condition and has several times
had gout in the right hand, but never at all
approaching in severity those she used to have
previous to the paralytic attack.

Three — Reproduction of gout by use of the
part. A gentleman fond of and accustomed to
pedestrian exercise has had many attacks of
acute gout in various parts. On two occasions
when the feet and ankles had been affected,
he, when he thought himself sufficiently re-
covered, walked several miles in heavy boots.
On both occasions acute gout was reproduced in
the parts which had been affected.

Four — Production of gout by pressure. The
familiar examples of this are found in cases

26 CHAPTEB II.

where gout in the great-toe is produced,
aggravated or reproduced by the pressure of a
too tight boot. Here is aa example of a
diflferent kind, which occurred in my own
person. At a certain stage of my knee attack
all symptoms had -disappeared except the
swelling, which was great and prevented the
knee from being flexed. I had occasion (before
I had left my bed) to drive for about an hour
into the country, see a patient and drive back
again. In my carriage, in order to avoid any
discomfort to the joint, I stretched the sound
leg straight out and placed the other limb upon
it as upon a splint. The outside of the right
heel rested upon the dorsum of the left foot
towards its outer edge. I came back and went
to bed, none the worse as regards the knee.
But in the course of an hour I felt pain in the
outer side of the right heel. On examination it
was found to be tender and brightly red over a
circular space larger than a half-crown. This
condition took three days to disappear. This it
may be said is a trivial instance of gouty

CHAPTER II. 27

inflammation. That is so. But any adequate
theory of disease must be able to explain trivial
just as much as the most portentous symptoms.
It may be asked, why, action and reaction being
equal and opposite, no efiect was produced
on the dorsum of the left foot ? Without under-
taking to answer that question in full it may be
pointed out, First — That the tissues of the heel
are dense and tense, while those of the other
part are lax. Second — That gout is common in
the heel, very rare in the other part. Third —
That gout was already manifested in the right
limb and not in the left.

It is generally recognised that gout may be
produced in joints by cold, and by wet feet.
And if producible it may be aggravated or
reproduced by the same agency.

Five — If such disorders as bronchial gastric or
intestinal catarrh may be gouty, as many
physicians besides myself think, there can be no
need to plead that cold may be an element in
their production as it is in non-gouty cases.

Six — Neuralgia and neuritis as distinct
and substantive disorders which are not always

28 CHAPTER 11.

distinguishable the one from the other are by
recognised authorities with whom I am in entire
accord, attributed in certain instances to the
gouty condition, or, to use another phrase, to
the gouty poison. Cold is often a factor in
their production.

Seven — In coming to such disorders as gout
in the stomach we are upon more debatable
ground. Sir Thomas Watson said he had often
found that " gout in the stomach " resolved itself
under the influence of an emetic " into pork " in
the stomach. To those who believe that gout
may be produced in the toe by the pressure of
a tight boot this dictum would go to prove, not
that these attacks were not gout, but that they
were gout, and gout produced by a sufficient
and ascertainable cause, viz., a local irritant.
That certainly is the eflfect produced upon my
mind.

Before leaving this part of my subject one or
two remarks. Is it not the case that external
agencies have not been sufficiently regarded as
gout producers ? That these cases have been

CHAPTER II. 29

looked upon rather as exceptions and oddities, .
without any special or deep significance ? If so,
that, insufficient inquiry has been made into
the minute history of gouty cases in respect to
previous or coincident injuries or other external
influences? Finally, if so, might not a more
constant and minute inquiry reveal a much
more constant relation between such external
circumstances and the appearance of gout in a
particular part ?

30

CHAPTER HI.

"TTTE now have to enquire into the nature of
" ^ the morbid condition of the local nerves
which is so frequently to be found in the vicinity
ot gouty manifestations, whether these be acute
and severe or subacute and slight.

Let us consider to what known pathological
conditions this affection is most akiu, having
regard to its clinical features. It is obvious
these resemble those of neuralgia, hyperaemia
of the nerves, and neuritis both acute and
chronic. Neuralgia has no pathological anatomy,
for the view which has been supported by some
authorities, viz — that it is in all cases due to
neuritis is not generally accepted. At the
same time it has an undoubted clinical existence,
and in some respects the features of this gouty
neuropathy resemble those of neuralgia. But

CHAPTER III. 31

little is known about hypereemia of the nerves
or its actual clinical occurrence. Erb remarks
on hypersemia of the nerves, that " it appears to
be deserving of some attention in the future,
since, perhaps, many so called functional
neuroses are referable to it."

Of neuritis both acute and chronic much
is known both clinically and pathologically.
Both neuralgia and neuritis are recognised by
the best authorities as occurring in gouty
persons and as being actually due to gout. Nor
are they as substantive diseases, that is as
existing independently of joint-gout at all rare
affections. An attempt therefore to give a new
significance to neuritis and to extend its domain
into parts where its existence has not hitherto
been recognised, is in accordance with, and not
hostile to, facts already known and accepted.

It will not be useless to state now some of
the facts of the natural history of acute neuritis.
And these I shall take almost verbatim from
the excellent article by Professor Erb in Von
Ziemmsen's Cyclopoedia of the Practice of
Medicine.

32 CHAPTER III.

Etiology. The most frequent and best known
causes of neuritis are wounds of various kinds,
contusion, rupture, &c. Slight mechanical
injuries may also cause neuritis, such as a blow
on a nerve trunk, strong compression of a nerve,
severe concussions of the nerves from long
travelling in an ill-constructed wagon, sudden
and violent muscular movements, violent efforts
to raise heavy weights, &c. It also arises from
" catching cold," exposure to a draught of air, &c.
Inflammations of various organs constitute a
very common cause of neuritis. After acute
diseases neuritic processes are not unfrequently
developed. Lastly, no one can wonder that it
is impossible in many cases to discover the real
cause of neuritis, and hence that we must speak
of its origin as spontaneous. It appears more-
over, as if many persons have a special
predisposition to neuritis, and especially as if
the disposition for the disease to spread upwards
or downwards along the nerves is present in
very different degrees in different individuals.
Special attention must be paid to this point in

CHAPTER in. 33

future." As regards the pathology of neuritis
much does not require to be said. In the earlier
stages there are microscopical evidences of in-
flammation in the neurilemma, then incipient
disintegration of the medulla and finally of the
axis cylinder. It may be taken that it is not in
all cases of neuritis that the inflammatory
process reaches to this last stage, and restoration
of the nerve may be established. We find that
there are two classes of change in these cases.
The one affecting the protective coverings of
the nerve ; the other affecting its conducting
apparatus. The two classes of change give rise
to two classes of symptoms. The one resembling
those common to inflammatory aflfections, the
other due to interference with, or abolition of,
the functions of the nerve as a conductor of
force. These vary according to the special
endowments of the nerve affected. When they
are of a trophic or vasomotor character, the
changes are also of that character, It remains
to mention one other feature of neuritis.
In whatever part in the course of a nerve it

34 CHAPTER ni.

originates, it has a tendency to spread both
downwards towards the periphery (neuritis
descendens), and upwards towards the centre
(neuritis ascendens). But according to all
authorities the ascending is much more common
than the descending form of extension. It is
also believed that without any upward extension
of the actual inflammation an influence may
ascend from the inflamed part upwards to the
cord, disturbing its functions and even causing
myelitis and its ordinary results. I will
not go into details respecting the chronic
form of neuritis, which may either be a primary
affection, or secondary to an acute attack. But
it may be well to draw the readers attention to
certain of the clinical features of neuritis and
neuralgia which find a distinct parallel in those
of gout.

Origin from injuries, and from cold.

Intensity of the pain.

Intensity of the tenderness over both the
trunk of the nerve and its peripheral distribution.

Pain and tenderness, the earliest symptoms.

CHAPTER III. 35

Radiation of pain towarfs periphery.

Remissions of pain.

Exacerbations tend to be nocturnal.

Pain auo;mented by every movement of the
part.

Cramps of muscles.

The (as a rule) more intense and early involve-
ment of sensory, as compared with motor, nerves.

Sensitiveness to pressure constant in neuritis.
Not constant in neuralgia.

Trophic disturbances of skin, nails and joints.

Hence glossiness of the skin in cases of long
standing.

Vasomotor disturbances.

It must not be forgotten that the conductivity
of the nerves may be impaired in quite another
way than by inflammation of the neurilemma.

Certain poisons introduced into the blood are
capable of producing a degeneration of the white
substance of Schwann and of the axis cylinder.
Of this the Diphtheria poison is an example.
It would be more correct to say the Diphtheria
poisons, for there are two, an ulbumose and an

36 CHAPTER in.

organic acid. Each of these, the albumose more
actively than the organic acid, is capable of
disintegrating motor, sensory, and sympathetic
nerves. Their action is firstly on the white
substance of Schwann and secondarily on the
axis cylinder, the neurilemma where that exists'
is but slightly if at all affected. Such at all
events are the conclusions drawn by Dr. Sidney
Martin, from his admirable investigations as
detailed in his Goulatonian Lectures (1892).

It seems to me probable that the painlessness
of Diphtherial paralysis is due to the absence of
changes in the neurilemma

i necessary to enumerate the many
)f gout which support the idea,
by CuUen, and now generally enter-
lat there is an intimate connection
his disease and the nervous system,
lot a treatise on gout but an effort to
: view that, granting this connection,
s peripheral nerves we must look for
id chief bond of union. I venture to
t what has been said will lead the

CHAPTER III. 37

reader to feel that after all it would not be very
surprising if this view should turn out to be
correct.

38

CHAPTER IV.

nnO give reasons, acceptable as it is hoped
-■- they may be, for thinking that there is
no inherent improbability, but the reverse, in
the neural element of gout being principally a
disorder of local nerves is not sufficient, it is
necessary to give reasons for thinking that it is.
Let us examine the two first cases which
I have described. One was a case of first
attack, in the other there was a history of
many previous attacks, of genuine gout occu-
pying its ordinary seat, the tarso-metatarsal
joint of the great toe. In each there was
evidence which would under any other circum-
stances be accepted as proof of the existence of
neuritis in close proximity to, indeed at one
extremity terminating at, the joint. Why

CHAPTER IV. 39

should this evidence not be accepted as equally-
conclusive in these cases ? It is a fact, at all
events it is accepted as one by all the best
modern authorities that neuritis occurs as an
isolated and distinct aflPection in gouty persons.
It is believed by the same authorities that it is
a manifestation of the gouty condition or poison.
In short, that there is truly such a thing as
gouty neuritis Is there then any inherent
improbability that it may occur not only as an
isolated affection but also in close connection
with another local gouty inflammation, that
namely of a joint ? Quite the contrary is the
case. " Inflammations of neighbouring organs,
extending to nerves traversing or adjoining such
organs, constitute a very common cause of
neuritis." (Erb). The fact then that neuritis
is to be found not only as an isolated affection,
but in close connection with the ordinary acute
joint-affection of gout, is important. The
bringing into close relation and proximity these
two reputedly separate affections is a distinct
step in an argument aiming to show that one is

40 CHAPTER^IV.

dependant upon the other. But it is quite in-
conclusive as to which is the primary and which
the secondary affection. Indeed if it points to
any conclusion, it is to one which is quite in
consonance with current opinion and accepted
fact6, viz. : that the neuritis is a secondary
inflammation set up hy a primary infiammation
of the joint.

But now let us turn to the consideration of
the other category of cases. It will probably
not be disputed that in the common opinion
they do not differ from acute attacks in kind
but only in degree. But what does an examin-
ation more searching and minute than ordinary
reveal 1 The presence of neuritis, the absence
of arthritis. The presence of a nerve disorder,
the absence of a joint disorder. The pnor
presence of a nerve disorder of a kind which is
admittedly capable of producing sensory, vaso-
motor, and trophic changes in parts which as a
nerve it supplies. The subsequent appearance
of such sensory vaso-motor and trophic changes.
There is here — it is right to point out — a link

CHAPTER IV. 41

at present missing. We may easily find
instances in which an acute arthritis has been
preceded by the minor pains and tenderness
which are, not ia the joint as has hitherto been
assumed, but in adjacent nerves. And I have
seen cases (two recently), in which there was
at the same time gouty affection of the thumb
without arthritis and gouty affection of the
fingers with arthritis and efiiision into some of
the knuckle-joints.

We want to trace a pre-existing neuritis
actually culminating in a frank attack of
arthritic gout. We can hardly expect to have
an opportunity of seeing this in our ordinary
patients. But there are many gouty medical
men. Is it too much to hope that they will
summon up courage enough to examine them-
selves, or to permit some one else to examine
them with minuteness in the first onset of
acute gout. The point to be determined is this.
Is there tenderness in the skin or in some of the
nerve-trunks surrounding the toe-joint at a
time when there is no tenderness in the toe-

42 CHAPTBE IV.

joint itself? The thumb or indeed any other
joint may be put to the question in a similar
manner.

It must however be remembered that such an

examination may be inconclusive. A neuritis

need not extend far from the joint, for the

effects of the suspension of nerve conduction

are the same in whatever portion of the

individual nerve fibre the obstacle occurs. Or

indeed if as in the arthropathy of tubes c

the nerve influence is affected at its

source. And if the skin to which it

is distributed be at the same time very tender

30 impossible to determine whether

is in the skin or in the joint.

e is this the case when the minute

a nerve itself is inflamed and lies

joint, for a slight movement of the

he, indeed often is, extremely painful

-he joint be evidently not affected.

her similar cases it may be impossible

■ certain that the pain is confined to

tarts and not also partly in the joint.

CHAPTER IV. 43

I hope indeed that all tlie clinical statements
upon which my argument is based may be
rigorously tested by those who have the
opportunity.

I venture now to claim to have established
a high degree of probability that in gouty
arthritis the joint affection is secondary to
and caused by a preceding (though possibly only
by a very short time) affection of the peripheral
nerves From this point of view a neuro-humoral
theory of Gout should be stated thus : —

In certain individuals, many of whom have a
parentage members of which have been similarly
affected, aberration of proteid metabolism occurs.
Its causes, origin and stages are unknown. The
most manifest of its terminal products is uric
acid. This in the form of quadriurate of soda
is present in the blood in abnormal quantity
and lowers its alkalinity. It is suspected,
though not decisively determined, that there
may be also present other terminal, collateral, or
bye products.

The circumstances under which this hypo — or
para — metabolism happens are excessive mental

44 CHAPTER IV.

•

strain especially if consisting of or accompanied
by anxiety or worry, excessive use of certain
kinds of food, or of alcohol, especially of
fermented malt liquors, or of strong or highly
saccharated or hyperacid, or effervescing wines
or those with a high percentage of sstherial
products. In consequence of this blood-state,
the stability of the nerve-trunks is impaired ;
and therefore their power of resisting external
influences which would be inoperative upon
normal nerves. These external influences are
the ordinary and still more the extraordinary,
use and effort of parts, concussion, and com-
pression of the nerves themselves, injury or
strain, irritants or cold.

The combined result of the intrinsic state of
the nerve trunks and of extrinsic influences is
the production of further changes in the nerves
notified by symptoms which are those either of
neuralgia or of neuritis, or of both, but the
anatomical basis of these has not as yet been
investigated.

The further effects of this neuropathy depend
first, on its intensity, second, on the endowments

CHAPTER IV. 45

of the nerve affected, viz., sensory, vaso-motor,
trophic, or motor, third, on the territorial
distribution of its ultimate branches, fourth, on
the involvement of two or more of the above
four classes of nerveg.

The blood poison seems to have an elective
affinity for the various classes of nerves in the
order in which they are above stated.

An increase, especially if it be sudden, in the
blood dyscrasia also enhances the neuropathy,
and may possibly be able to induce it without
the co-operation of any external cause. Such
increase may be due to —

First — Aggravation of the primary cause of
the altered metabolism and consequent increase
of morbid products.

Second — Liberation into the blood of such
products which had been previously stored up
in some part or viscus.

Third — Diminution of the eliminative power
of some organ or organs by which these products
had been previously separated from the blood.

It is probably under one of these heads that is
to be classed a general perturbation of the system.

46 CHAPTER IV.

The neuropathy has the following qualities in
common with neuritis, that of ascending or
descending from its primary seat, unless that be
in the ultimate fibrils when it necessarily has
an ascending power only. In common with
neuritis and neuralgia, that of affecting the state
of the spinal {and possibly of higher,) centres
and radiation thence to other nerve territories.

The highest and lower cerebral centres must

be credited with the power of originating or

aggravating the general gouty condition.

Conceivably through their known potentiality

over recognised seats of metabolic activity.

r perhaps also be credited with the

determining local outbreaks. Con-

hrough tbeir known potentiality over

especially vaso-motor nerves. The

ect being due to the altered conduct-

le affected peripheral nerve.

Ii cerebral centres are also liable to be

' the blood dyscrasia (e.g., ill temper,

a), but in what way this is brought

e is no evidence to show.

CHAPTER TV. 47

There is no doubt that a biurate salt may be
deposited in some of the viscera aflPected by
localised gout. Such a deposition is usual when
the part aflFected is a joint. This is by no means
a necessary or invariable result, according to the
only evidence at our disposal. For while on the
one hand the deposit has been found many
years after a joint had been affected once only,
on the other none has been discoverable in a
joint which had been many times affected.
This deposit must be looked upon as an
epiphenomenon. And its presence is probably
due to the peculiar mode in which joints are
nourished. The amount of deposit is, speaking
generally, in inverse proportion to the acuteness
of the other symptoms, and therefore less in the
earlier attacks and greater in the later ones.
It may also take place in the absence of any
preceding or concomitant pain, or redness, or of
any swelling except that which itself produces.
An attack in a joint is sometimes followed by a
cessation of extraneous symptoms which we
suppose to depend upon the abnormal state of

48 CHAPTER IV.

the blood. When this is so it would appear that
it is either evidence, or the cause, of a reversion
to normal metabolism, but in what way this
result is produced we have no evidence.

49

CHAPTEK V.

A THEORY however specious is valueless
-^^^ except in as far as it is based on facts,
which it not only recognises but harmonises.
It may I think be fairly claimed for this theory
that it harmonises and brings into line a greater
number of the admitted facts of Gout than any
other. It does not fail to recognise that there
are important elements of the disease the
nature of which is as yet concealed from our
eyes. But it is not in hostility to any
admitted facts.

It recognises two great classes of facts.
First — Those which have for ages been seen
to indicate that the fluids of the body are
concerned in the production of gout and which
are therefore the basis of the humoral theory.

50 OHAPTEB V.

Second — Those which indicate that the
nervous system is concerned in the production
of gout, and are the basis of the neural or nerve
theory of gout.

This latter since the time of Cullen has

always held a distinct though fluctuating hold

of medical opinion. Of late years these two at

one time opposing theories have been more or

less held in conjunction. As indeed it seems to

me they must be, unless we ignore some of the

most prominent features, and best ascertained

facts of the disorder. The weakness of the

nerve theory haa hitherto been its vagueness.

And this has materially retarded its general

acceptance. To this hitherto almost abstract

proposition the localisation of the nerve element

in a definite section of the nervous system gives

concreteness. To many minds " the nervous

relation, means nothing.

ich they can grasp. There

such difficulty in regard to

at least provisionally term

ne a tangible basis is given

CHAPTER V. 51

to the nerve theory and thus should commend
my theory to the holders of that view. Nor
have I excluded the possible co-operation of the
spinal centres. On the contrary it has been
pointed out in what way they may be affected.
And this way is in accord with the teachings of
general pathology. Similarly it has been pointed
out in what way the highest centres may have
an influence, though it remains for the future to
show in what way or ways their influence is
actually exercised and the results of such
exercise. It is to be borne in mind that if no
more precise explanation is offered here neither
is one offered elsewhere.

So much for general considerations in favour
of the theory which I have presented. Let us
now look at some particular ones.

How does this suggested theory fit in with
known clinical facts ? Foremost of these is the
immense preponderance of attacks of acute gout
in the tarso-metatarsal joint of the great toe as
compared with any other joint. Any theory of
gout which does not explain this fact is

52 CHAPTER V.

inadequate, even if it is not so far as it goes
erroneous. How is this explained at present.
Firstly — by the remoteness of the part from the
centre of circulation. Secondly — by pointing
out that the whole weight of the body rests in
walking upon this joint. As regards the circu-
lation it is no more remote than that of tlie
corresponding joints of the other toes As
regards the weight of the body. In the first
place, the weight of the foot, which is insig-
nificant in proportion to the total body weight
is the only burden which the toe bears in excess
of that which is borne by the ankle.

But the whole weight of the body does not
rest upon the great toe. It is divided between
that and the other toes, the combined area of
whose tarso-metatarsal joints cannot be much
less, even if it is not more than that of the
great toe-joint. But between this and the other
toes there is this difference. The nerves around
the great toe joint are not deeply seated in
the soft parts, they are subject to pressure on
the sole aspect by the weight of the body, on

CHAPTER V. 53

the inner and upper aspects by the upper leather
of the shoes. Whereas the nerves of the other
toes which are rarely attacked are protected by
the soft parts and by the cushion of the sole
and are in most boots much less pressed upon
than the great toe by the upper leather. I
submit then that a local nerve theory of gout
affords a satisfactory explanation of this clinical
fact, which current views do not.

It is known that repeated attacks may
occupy a great toe-joint which on subsequent
examination does not show any uratic infiltra-
tion. It seems to me probable that in an
ordinary attack there are two elements. An
inflammation of the joint, and an inflammation
of the neighbouring soft parts. On the nerve
theory and having regard to the nerve distribu-
tion we can understand this and we can suspect
that one element may occur without the other.
It is indeed a matter of inference, rather than
of observation, in many cases, that the joint has
been affected at all. On the other hand we
know that in old cases where the joint

54 CHAPTBE T.

destruction and infiltration proceed most actively
the inflammation of the soft parts is commonly
at a minimum. The same is true of the other
joints. We see also uratic deposits formed in
parts which have never, so far as we can judge,
been the seat of any inflammatory process. Or
if of any, it has been of the slightest and most
transient character.

It is known that tophi are very common in

the ear. This may be due partly to cold but

more I think to pressure. They are usually

accompanied or preceded by very slight in-

f symptoms, often by none. The

8 made by the weight of the head
ig them against tbe pillow in bed.
especially when the ear is doubled up
happens. We then get mechanical
,he outside, and strain on the inside
the auricle. In other words pressure

9 pressure and stretching on the other.
at infrequency of gout in the hip-joint
ommented on by writers. I suggest
s due to the great protection from cold

CHAPTER V. 55

and external injury afforded to its nerves by
the depth at which they Ue in a mass of soft
parts. The sciatic nerve itself from which one
at least of these nerves springs at a high level,
is on the contrary much exposed to both cold
and pressure and is a common seat of gouty
affection. The shooting pains, the localised
tendernesses are equally explicable. So also the
cramps, often a most troublesome symptom.

It is well-known that the most acute attacks
of toe-gout may be made to disappear with
great rapidity. One method which has been
adopted — amongst others by the great Harvey
in his own case — ^is to plunge the foot into cold
water. Another is by giving freely of colchicum.
There are others, but these two will suffice.
Now if the inflammation of the great toe be
caused by a deposition of a uric salt in the
cartilage, a condition which is known to be
extremely stable, we have great difficulty in
seeing how its removal may be effected in so
short a time. On the other hand we know that
the phenomena of neuritis and still more of

56 CHAPTER V.

neuralgia are exceedingly inconstant, that they
may appear and disappear spontaneously with
great suddenness. We thus have an explan-
ation, which at least is not incomprehensible, of
the effect of such agents as cold and colchicum
upon acute gout. To those who hold that
colchicum is a drug which acts, not as an
eliminant, but directly upon some part of the
nervous system, this explanation appeals with
superior force. It affords indeed a strong
argument in support of their view. It is also
worthy of notice that Weir-Mitchell insists
strongly on the free application of ice in con-
gestion of nerves.

Let us now briefly consider the bearing of

this view upon the various gouty affections of

internal organs. In the first place it cannot be

denied that, while the existence of such disorders

is fully recognised by many of us, it is very

' * ^ ' admitted by a considerable school

nion is not to be treated with, nor

jition removed by, contempt.

seems to me that this opposition has

irisen from a conception of gout.

CHAPTER V. 57

postulating for its existence the tissues of a
joint. It is from this conception that have
arisen the terms of regular and irregular gout.
There is not much analogy between the special
tissues of a joint and those of a mucous
membrane. Into a mind dominated by the idea
that without a joint localised gout is not possible
it is easy to see that the idea of gout in a
mucous membrane will enter with diflficulty.
But with the admission of the idea that the
starting point of a localisation of gout is an
affection of the local nerves, this dijB&culty is
removed. It enables us also to answer definitely
questions which I have often had put to me by
a colleague in a consultation in some such
form as this. "Here is a case of bronchial
catarrh, with all the ordinary physical signs and
symptoms. What do you mean by saying it is
' gouty ' ? Do you think that all bronchial or
other catarrhs are gouty ? " These or suchlike
questions put in good faith require an answer,
which I have hitherto given as follows. " I do
not consider all bronchial or other catarrhs to

58 GHAPTER V.

be gouty; not necessarily so even when one
occurs in a person who has had gout. By gouty
catarrh I mean a catarrh which has for one of
its factors the gouty poison in the blood. The
reason I think this particular case is in this
category is, firstly, because your treatment, very
proper for a case of simple bronchitis, has failed.
It has failed because it has not removed the
gouty factor. Secondly, because there are now
present, or quite recently have been, symptoms
which are common in gout, from which I infer
that this patient is in a gouty condition.
Thirdly, I have known many cases of catarrh
which have not been relieved till the treatment
has been based upon this view." I should now
make this explanation more definite, and there-
fore more acceptable by saying that the
persistence of the disorder was due to the
deterioration of the local nerves by the agency
of the gouty poison.

This explanation is applicable to any one of
the multifarious manifestations of gout. At all
events in any part the nerves of which are

r

CHAPTEB V. 59

covered by a neurilemma. Whether or no gout
poison can act directly upon naked nerves is a
matter for future examination.

It is much to be hoped that the evidence of
local nerve disorder in localised gout which I
have collected may lead to an investigation of
the state of these nerves by some of our younger
pathologists, who have the necessary accomplish-
ments and time at their disposal. Is this
disorder due to neuritis, to congestion, to
primary degeneration or to the changes, what-
ever they may be, which produce the state
known to us as neuralgia. Clinical features may
be recognised which might be explained by any
one of these, and are especially in accord with
congestion, neuralgia and neuritis.

The theory I have advocated forms a definite
basis for the neural element of neuro-humoral
theory of gout and brings into one line a
greater number of the clinical features of gout
than any other one. I commend both it and
the facts on which it is based to the candid
consideration of the profession.

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